Extracellular brain ammonia levels in association with arterial ammonia, intracranial pressure and the use of albumin dialysis devices in pigs with acute liver failure.

In acute liver failure (ALF) hyperammonemia plays a mayor role in the pathogenesis of hepatic encephalopathy (HE) but does not always correlate with the severity of mental deterioration and intracranial pressure (ICP). The aim of our study was to evaluate the association with extracellular brain ammonia, ICP and the therapeutical impact of two albumin dialysis devices. ALF was induced by complete hepatectomy in 13 pigs. All pigs were monitored and treated under intensive care conditions until death. Arterial blood and cerebral microdialysis samples were collected and ICP data recorded. Additionally in 5 pigs, standard albumin dialysis and in 3 animals an albumin dialysis prototype was initiated as a tool. Arterial ammonia increased straight after hepatectomy, while extracellular brain ammonia remained on a moderate level 10 h post ALF initiation. After 16 h the brain ammonia reached arterial ammonia levels before plateauing at 1,200 microM, though the arterial ammonia continued to rise. The ICP correlated with the brain ammonia levels. No impact of the different dialysis therapies on neither blood nor brain ammonia levels was observed. In ALF the extracellular brain ammonia revealed a delayed increase compared to arterial ammonia. It correlated strongly with the ICP and could serve as a sensitive marker for HE development. Albumin dialysis did not affect blood or brain ammonia levels.